Mismatching of ventilatory output to the central respiratory output (19) and autonomic dysfunction (67,84,99) has been implicated in both asthma (67,84) and cystic fibrosis (99). Our objective is to study two indices of central inspiratory activity; 1) the electrical activity of two accessory muscles of respiration that serve to stabilize the upper airways prior to inspiration (16,106) and 2) the modulation of heart rate by breathing pattern, the "respiratory sinus arrhythmia," an index of the balance between parasympathetic and sympathetic cardiac control (59). We shall study these indices of respiratory center output and autonomic function in young, normal humans during standard ventilatory perturbations that alter afferent activity to the respiratory centers and compare their results to those of age-matched patients with chronic obstructive pulmonary disease (COPD). 1) Fine wire electromyography (EMG) of the dilator naris and genioglossus muscles will be used to study the behavior of single motor units (SMUs) to ventilatory loads and chemostimuli, and to determine the temporal relationship of neuromuscular to mechanical (flow and pressure) events. Analysis of SMU firing profiles will enable us to determine whether increases in global EMG activity are mediated by changes in SMU firing profiles, the order of recruitment of new units, or both 2) Normal subjects and patients with COPD will voluntarily control tidal volume and breathing frequency (53) or breathe spontaneously on the ventilatory stresses used in the EMG study. By spectral (8,30,55) and frequency (120) analysis the contributions of respiration, periodicities in blood pressure, muscle blood flow, and end-expiratory lung volume (54) to heart rate modulation. Comparison of control of heart rate and central respiratory output in health and COPD will provide a non-invasive index of autonomic balance and therefore, a clinical tool to evaluate the integrity of the cardiorespiratory control centers. Basic knowledge of the mechanisms governing the respiratory output and cardiorespiratory interactions in health and COPD will afford a better understanding of the pathophysiology of CPOD with potential improvement in therapy through a rational approach.